
Low hematocrit and hemoglobin chf manual#
Merck Manual Professional Version: Overview of Hemolytic Anemia.Merck Manual Professional Version: Sideroblastic Anemias.Cleveland Clinic Center for Continuing Education: Anemia.Hemolysis may likewise result from direct trauma to RBCs as blood flows through artificial heart valves or past blood clots within blood vessels. Certain bacteria, such as meningococci and streptococci, produce toxins that directly destroy RBCs. In some autoimmune diseases, hemolysis occurs when the body makes antibodies that attack its own RBCs. In hypersplenism, the spleen is overactive and destroys an excessive number of RBCs. Hemolysis may also be caused by disorders outside RBCs. This leads to hemolysis during acute illnesses, such as infections, or upon exposure to fava beans or certain drugs. In glucose-6-phosphate dehydrogenase (G6PD) deficiency, RBCs are unusually susceptible to harmful oxidizing molecules. In diseases with abnormally shaped RBCs, such as sickle cell anemia or spherocytosis, the body identifies the cells as abnormal and destroys them prematurely. Hemolytic anemia develops when RBC destruction occurs before this time and the bone marrow is unable to release enough new cells.

RBCs remain in the bloodstream for about 120 days, after which they are destroyed - primarily in the spleen - and replaced by new RBCs released from the bone marrow.

Infiltration of the bone marrow by fibrous tissue or cancer cells likewise interferes with RBC production.

In aplastic anemia, for example, the entire bone marrow stops producing RBCs and anemia may be severe. RBCs are produced in the bone marrow, so any disease within the marrow may cause anemia, depending on the extent of bone marrow affected.
